Brazil nuts improve lipids, oxidative stress and blood vessel function in obese adolescents

Summary: Brazil nuts protect against vascular disease in overweight female adolescents.

Recent research published in the journal Nutrition & Metabolism offers evidence that Brazil nuts, besides being more effective at raising serum selenium levels than selenium taken as a supplement, improve the lipid profile and protect against blood vessel damage. The authors state:

Obesity is a chronic disease associated to an inflammatory process resulting in oxidative stress that leads to morpho-functional microvascular damage that could be improved by some dietary interventions. In this study, the intake of Brazil nuts (Bertholletia excelsa), composed of bioactive substances like selenium, α- e γ- tocopherol, folate and polyunsaturated fatty acids, have been investigated on antioxidant capacity, lipid and metabolic profiles and nutritive skin microcirculation in obese adolescents.”

Their study subjects comprising obese female adolescents were randomized to a group that consumed 15-25 g/day of Brazil nuts in capsules for 16 weeks and a placebo group. Anthropometry, metabolic-lipid profiles, oxidative stress, capillary diameters, functional capillary density, red blood cell velocity (RBCV) were measured at baseline (T0) and after the Brazil nut intervention (T1). What did the data show?

“At T1, BNG [the Brazil nut group] had increased selenium levels, RBCV and RBCVmax and reduced total (TC) and LDL-cholesterol. Compared to PG [placebo group], Brazil nuts intake reduced TC, triglycerides and LDL-ox and increased RBCV.”

In other words, compared to the placebo group, the Brazil nut cohort had better blood vessel function, lower total and LDL cholesterol and, importantly, reduced oxidized cholesterol (LDL-ox, the truly ‘bad’ cholesterol). Naturally, they also had higher selenium levels. The authors conclude:

Brazil nuts intake improved the lipid profile and microvascular function in obese adolescents, possibly due to its high level of unsaturated fatty acids and bioactive substances.

Fasting before blood tests may not be necessary for children

With the unprecedented expansion of overweight, obesity and pre-diabetes in the pediatric population it is becoming increasing important to evaluate metabolic status with appropriate blood tests at a younger age. Anything that makes this task less onerous is desirable. A welcome study just published in the journal Pediatrics offers evidence that fasting may not be necessary to reliably evaluate lipid status in children. The authors state:

“Fasting lipid panels are recommended to screen for lipid abnormalities; however, fasting can be difficult for children and make screening difficult. Results of studies in adult patients are raising questions of whether fasting is needed before lipid screening.”

They examined total cholesterol (TC), HDL (high-density lipoprotein), LDL (low-density lipoprotein), and triglyceride cholesterol components in relation to fasting in 12,744 children aged 3 to 17 (varying times for young children and the usual fasting for those older than 12 years). The data appear to give kids a break:

“TC, HDL, LDL, or triglyceride values were available for 12 744 children. Forty-eight percent of the TC and HDL samples and 80% of the LDL and triglyceride samples were collected from children who had fasted ≥8 hours. Fasting had a small positive effect for TC, HDL, and LDL, resulting in a mean value for the sample that was 2 to 5 mg/dL higher with a 12-hour fast compared with a no-fast sample. Fasting time had a negative effect on triglycerides, which resulted in values in the fasting group that were 7 mg/dL lower.”

Furthermore…

“For TC, nonfasting screening inappropriately classifies ≈1% of children as normal, who would have had borderline values with fasting. In addition, ≈1% of children with borderline nonfasting values would actually have elevated results if fasting. For LDL, 1.2% of children with borderline fasting levels would have normal results postprandially, and 1.6% of children with increased calculated LDL while fasting, would now be considered to have borderline results. For triglycerides,≈4% of the children classified with normal triglycerides when fasting would have elevated values postprandially.”

In other words, most of the time the difference between fasting and non-fasting in children is not clinically significant.

The authors conclude:

“Comparing a nationally representative cross-section of children who had fasted for various lengths of time, we demonstrated that nonfasting measurements of TC, calculated LDL, and HDL cholesterol values had only small differences from fasting values. Although statistically significant, these differences are unlikely to result in important clinical changes in the results of screening for cholesterol abnormalities. …Across a large, nationally representative sample of children, the levels of TC, HDL, non-HDL cholesterol, and LDL cholesterol vary minimally on the basis of fasting time. It is not known if these small differences in lipoprotein components consistently weaken or strengthen the usefulness of lipid values for the assessment of current health risks or prediction of future cardiovascular risks, but it is clear that testing regardless of fasting status would reduce barriers to screening. Therefore, future research with people in longitudinal samples is warranted. If those results confirm our findings, professional societies might wish to reconsider their recommendations and encourage providers follow lipid screening guidelines at the point of care, regardless of fasting status.”

It will be helpful if future studies can offer data specifically quantifying the impact of fasting versus non-fasting on subsequent cardiovascular and metabolic risks. However, on the basis of the evidence we have now, my personal preference is to make it as easy on the kids as possible. Fasting a galloping pediatric metabolism risks a low blood sugar state that is not only globally miserable but elicits a vasoconstrictive autonomic response that makes phlebotomy much more difficult and traumatic.

Cholesterol levels vary with the menstrual cycle

A study recently published in The Journal of Clinical Endocrinology & Metabolism proves that we must take the menstrual cycle into consideration when testing cholesterol in cycling women.

“The objective of the study was to evaluate the association between endogenous [internally produced] estrogen and serum lipoproteins across the menstrual cycle.”

The authors found that total and LDL cholesterol were lower during the luteal phase (second half, when progesterone is higher) than the follicular phase:

More women were classified above the desirable range (LDL ≥130 mg/dl or total cholesterol ≥200 mg/dl) when measured during the follicular phase [first half].”

HDL was higher when estradiol had peaked, corresponding also to lower LDL and triglycerides.

Because lipoprotein cholesterol levels vary across the menstrual cycle, cyclic variations in lipoprotein levels may need to be considered in the design and interpretation of studies in reproductive-age women and in the clinical management of women’s cholesterol.

More reasons to go nuts for heart disease

Archives of Internal MedicineA paper just published in the Archives of Internal Medicine analyzes the evidence from 25 intervention trials on the effect of eating nuts on blood lipid levels and heart disease. The authors begin by noting:

Epidemiological studies have consistently associated nut consumption with reduced risk for coronary heart disease…The objectives of this study were to estimate the effects of nut consumption on blood lipid levels and to examine whether different factors modify the effects.”

They pooled the data from 25 trials in 7 countries for cholesterol, LDL, ratio of LDL to HDL, and triglycerides. Improvements were documented in all of these factors. The data also showed that:

“The effects of nut consumption were dose related, and different types of nuts had similar effects on blood lipid levels…the lipid-lowering effects of nut consumption were greatest among subjects with high baseline LDL-C and with low body mass index and among those consuming Western diets.”

In other words, eating more nuts improved the lipid-lowering effect. Hence their conclusion:

Nut consumption improves blood lipid levels in a dose-related manner, particularly among subjects with higher LDL-C or with lower BMI.”

Sugars raise bad fats in the blood

JAMAReaders and patients here know how higher levels of insulin from a high glycemic diet can result in an increase in the harmful kinds of fat in the blood. It will come as no surprise that a paper just published in the Journal of the American Medical Association adds more evidence to the association. The the objective of the authors was to…

“…assess the association between consumption of added sugars and blood lipid levels in US adults.”

They analyzed the data for 6,113 adults collected over seven years for sugars in the diet and levels of HDL and LDL cholesterol and triglycerides. A clear correlation between higher levels of sugars and lower HDL (“good” cholesterol), higher LDL (“bad” cholesterol) and higher triglycerides emerged. There was strong evidence for maintaining a low glycemic diet to regulate cholesterol:

Among higher consumers (≥10% added sugars) the odds of low HDL-C levels were 50% to more than 300% greater compared with the reference group (<5% added sugars).”

Their conclusion was mildly stated:

“In this study, there was a statistically significant correlation between dietary added sugars and blood lipid levels among US adults.”

Journal of Lipid ResearchHave you been trying but not succeeding in getting cholesterol and/or triglycerides down with a low fat diet? There has been so much science done on the correlation between insulin sensitivity and cholesterol levels; it’s surprising this wasn’t noted by the authors. Just one example is a fresh paper in the Journal of Lipid Research that begins with the well-known fact:

“Cholesterol synthesis is upregulated and absorption downregulated in insulin resistance and in type 2 diabetes.”

Interestingly, the authors wanted to see if any level of insulin resistance would have an effect on cholesterol synthesis:

“We investigated whether alterations in cholesterol metabolism are observed across the glucose tolerance status, from normoglycemia through impaired glucose tolerance to type 2 diabetes…”

What conclusions did they draw from their data?

“In conclusion, cholesterol metabolism was altered already in subjects with impaired fasting glucose. Upregulated cholesterol synthesis was associated with peripheral insulin resistance independent of obesity.”

How to eat healthy fat and oil is another topic, but if cholesterol and triglycerides are the issue—pay attention to sugars and insulin.

Fructose even worse than glucose for fat and insulin

Journal of Clinical InvestigationThis is why the ubiquitous high-fructose corn syrup is such a disaster for public health. The authors of this study published in The Journal of Clinical Investigation note that “Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance.” When they examined the effect in humans they found that all the following were increased markedly in the subjects on fructose but not glucose: visceral adiposity (fat around the organs), plasma triglycerides, fat in the liver, small dense LDL, oxidized LDL, fasting glucose and fasting insulin. At the same time insulin sensitivity decreased in the subjects consuming fructose but not glucose. The authors conclude: “These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.” [DNL = de novo lipogenesis which means making fat from scratch in the liver.] An accompanying commentary in the same journal states: “In the event that any readers harbor some remaining skepticism, an unprecedented thorough analysis in close to 900,000 participants from almost 60 prospective studies was very recently published, proving beyond any possible doubt that progressive excess mortality is caused by increased body adiposity…Stanhope and colleagues provide major scientific progress by demonstrating marked differences in the metabolic effects of these two major sugars with respect to their ability to promote intraabdominal lipid deposition and hepatic lipid production, while shifting cholesterol metabolism in an unfavorable manner and diminishing insulin sensitivity in humans.” Public health is groaning under a burden of overweight/obesity; how much disease could we prevent just by cutting out most of the sweet drinks (including most fruit juices) for children and adults?